Among cognitively normal people with amyloid plaques, women have more tau tangles in the entorhinal cortex than do men. Does this indicate susceptibility, or resilience?
In cognitively normal people, a set of blood proteins may predict whether or not amyloid plaques have deposited in a person’s brain.
The FDA has prioritized review of C2N’s blood test for amyloid-β. A pivotal clinical trial will correlate the test with amyloid PET scans.
Studies in mice and humans show that sleep suppresses extracellular tau and slows its spread.
In familial Alzheimer’s disease, rise in NfL in the blood precedes disease onset by 16 years.
Stakeholders have until February 11 to comment on draft FDA guidance for biomarker qualification.
During deep sleep, people with AD pathology, particularly tau tangles, have less low-frequency slow-wave brain activity, which is important for memory consolidation.
The largest study so far to compare brain scans and CSF among African-Americans and Caucasians finds differences, but participant numbers remain small.
The ligand binds the microglia-specific CSF1 receptor in animal and postmortem studies; human trials are forthcoming.
This past year, therapeutic antibodies massively reduced brain amyloid, blood tests came into their own, and systems-based approaches transformed the study of gene expression, glial cells, and selective vulnerability.
An ultrasensitive assay picked up elevated concentrations of N-terminal tau fragments in the blood of people with AD.
Case study in early onset AD finds PET ligand tracks regional tau burden.
In patients across a range of neurodegenerative diseases, NfL ramps up in the cerebrospinal fluid. Levels are higher in those with worse disease.
FDG PET revealed the formation of a new functional brain network. It explains clinical improvements noted previously.
In sporadic and familial forms of AD, progranulin climbs in the cerebrospinal fluid as disease progresses, perhaps reflecting microglial activation.